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What are the 3 types of rodenticides?
- anticoagulant rodenticide: hydrocoumarins, indanediones
- neurotoxin rodenticide: bromethalin
- hypercalcemia (vit D3) rodenticide: cholicalciferol
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What are the 2 most important factors to determine when dealing with rodenticide toxicity?
- what type of rodenticide was ingested
- when was the first possible exposure
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What is the mechanism of toxicity of anticoagulant rodenticides?
blocks vitamin K reductase, causing cavitary bleeding
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Describe the toxicokinetics of anticoagulant rodenticides.
- readily absorbed from GI tract
- peak blood level in 1-12 hours
- undergoes enterohepatic recycling
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What are clinical signs of anticoagulant rodenticide toxicity? (3)
- clinical hemorrhage 2-3 days following ingestion
- cavitary bleeding most common
- hemorrhagic shock
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What is the earliest test to determine if a patient has consumed a toxic dose of anticoagulant rodenticide?
PT (which tests the extrinsic coagulation pathway, factor VII, which has the shortest half life)- will be prolonged PT at 48 hour mark if a toxic dose was consumed
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How do you identify acute anticoagulant rodenticide toxicity?
alteration in coagulation times and clinical signs will not yet be present b/c carboxylates vit K factors will still be present in circulation
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What is the treatment for acute ingestion of anticoagulant rodenticide?
- emesis
- decontamination- repeated activated charcoal for 24 hours
- if PT is prolonged at 48 hour mark without clinical bleeding--> oral vit K supplementation for 30 days (recheck PT 48 hours after discontinuing vit K)
- WITH clinical bleeding--> fresh frozen plasma, frozen plasma, cryosupernatant, whole blood, packed RBCs
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What are the goals of treating the bleeding patient after anticoagulant rodenticide toxicity? (3)
- replacement of active vit K dependent clotting factors
- replace exogenous vit K
- replace RBCs if bleeding severely
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Describe the properties of fresh frozen plasma, frozen plasma, cryosupernatant, whole blood, and packed RBCs.
- FFP: contains all clotting factors
- frozen plasma: contains factors II, VII, IX, and X
- cryosupernatant: contains factors II, VII, IX, and X
- whole blood: contains RBCs, all clotting factors, and platelets
- packed RBCs: only for red cell replacement
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What is the mechanism of toxicity with neurotoxic rodenticide?
inhibits oxidative phosphorylation--> decreases ATP production in the CNS--> malfunction of ATP-dependent ion pump--> influx of sodium and fluid--> cerebral edema
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Describe the toxicokinetics of neurotoxic rodenticide.
- enterohepatic recycling
- very long half life/ prolonged effects
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What are clinical signs of neurotoxic rodenticide toxicity with acute lethal ingestion? (7)
- [within 2-24hrs]
- CNS stimulation or depression
- abnormal behavior
- hyperesthia
- hyperthermia
- focal or generalized motor seizures
- CNS abnormalities
- hind climb paralysis, ataxia, tremors
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What are clinical signs of neurotoxic rodenticide toxicity with chronic low dose exposure? (8)
- ataxia
- paresis
- loss of proprioception and deep pain
- hyperreflexia
- UMN bladder
- mild to severe CNS depression
- focal or generalized motor seizures
- abnormal body postures (schiff-sherrington, decerebrate)
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What is the acute toxic dose of neurotoxic rodenticide?
0.25-1mg/kg
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What is the treatment for neurotoxic rodenticide ingestion? (5)
- emesis (if exposed within the last 2-4 hours)
- decontamination (repeated activated charcoal for 24-48 hours)
- mannitol (decrease cerebral edema)
- anticonvulsant therapy
- methocarbamol for tremors
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What is the mechanism of toxicity for hypercalcemic rodenticide?
high dose of cholecalciferol results in increased Ca absorption, increased urinary Ca reabsorption and increased bone mineralization--> severe hypercalcemia
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Describe the toxicokinetics of hypercalcemic rodenticides.
- enterohepatic recycling
- terminal half life is weeks to months due to high fat solubility
- hypercalcemia can persist for weeks
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What are clinical signs of hypercalcemic rodenticide toxicity? (7)
- [usually 36hr post ingestion]
- depression/ weakness
- GI upset
- PU/PD
- lethargic
- acute renal failure
- cardiac arrhythmias
- seizures
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What is the treatment of hypercalcemic rodenticide toxicity?
- emesis
- decontamination (repeated activated charcoal for 24 hours)
- reduction of hypercalcemia with fluid therapy, furosemide, +/- calcitonin, bisphosphonates (decreases osteoclastic behavior), steroids (reduce GI absorption of Ca), phosphorous binders
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What is the mechanism of toxicity of pyrethrins/pyrethroids?
reversible neurotoxin that alters the voltage sensitive sodium channel, leading to disruption of their function
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Describe the toxicokinetics of pyrethrins/ pyrethroids.
- fat soluble
- toxicity enhanced by carriers (alcohols, solvents)
- cats are more sensitive
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What are the clinical signs of pyrethrin/ pyrethroid toxicity? (12)
- immune-mediated hypersensitivity- dermal manifestation
- neurotoxicity- muscle tremors, ataxia, seizures, death
- topical and oral stimulation- hypersalivation, paw flicking, ear twitching, hyperesthia, decreased activity, vomiting, diarrhea
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What is the treatment for pyrethrin/ pyrethroid toxicity? (5)
- oral exposure- decontaminate
- allergic skin reaction- diphenhydramine
- neurologic reaction- muscle tremors treated with methocarbamol, seizures treated with anticonvulsants
- aggressive supportive care
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What is the mechanism of toxicity of carbon monoxide?
- CO binds hemoglobin to create carboxyhemoglobin, blocks binding of oxygen--> cellular hypoxemiaÂ
- direct cytotoxicity due to altered cellular respiration--> free radical formation--> cell death
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What are clinical signs of carbon monoxide poisoning?
- dyspnea
- nausea/ vomiting
- dizziness
- tachycardia
- arrhythmias
- weakness
- ataxia
- seizures
- syncope
- hypotension
- red MMs
- coma
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How is CO poisoning diagnosed? (2)
- CO-oximetry: confirms CO toxicity by measuring the amount of hemoglobin, oxygen saturation, and percentage of CO-Hgb
- arterial blood sample: PaO2 will represent dissolved oxygen in blood d/t oxyhemoglobin curve being shifted to the left; monitor response to therapy this way
- [pulse ox: not accurate, CO-Hgb absorbs the same wavelength as O-Hgb]
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What is the treatment for CO toxicity? (2)
- oxygen supplementation
- supportive care
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What is the mechanism of toxicity with ethylene glycol?
- EG itself is not toxic
- its metabolites from the liver result in clinical disease by forming oxalates, which are nephrotoxic and result in mineralization of renal tissue
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What are clinical signs of ethylene glycol toxicity, separated by timeframe?
- 30 min: nausea and vomiting, CNS depression, ataxia, LMN signs in limbs, muscle fasiculations, PU/PD
- 24-72 hours: signs of AKI- depression, anorexia, vomiting, seizures, pytalism, oral ulceration, and coma
- 72-96 hours: anuria, cats may have swollen painful kidneys
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How is ethylene glycol toxicity diagnosed? (7)
- history
- elevated osmolal gap (1 hour following ingestion and remain elevated for 18 hours) [2(Na+K) + (BUN/2.8) + (glucose/18)]
- high anion gap (within 3 hours of ingestion) [(Na+K)- (Cl+HCO3)]
- urinalysis: calcium oxalate crystals (within 3-6 hours), isosthenuria
- also EG test kits available
- biochem: azotemia, hyperPh, hyperK
- abdominal US: halo sign/ hyperechoic renal cortex
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What is the treatment of ethylene glycol toxicity? (3)
- 4-MP or fomepizole (alcohol dehydrogenase inhibitor, block conversion of EG to toxic metabolites)
- ethanol 20% (competitive substrate for alcohol dehydrogenase, bloc conversion to toxic metabolites)
- hemodialysis (remove EG and toxic metabolites)
- [note: decontamination NOT helpful]
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